Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

A, Jie Wang; Tang, Yufeng; Zhang, Jingjing; B, Jie Wang; Xiao, Mengjie; Lu, Guangping; Li, Jiahao; Liu, Qingbo; Guo, Yuanfang; Gu, Junlian

doi:10.1016/j.redox.2022.102310

Cited by 40 publications

(30 citation statements)

References 54 publications

(69 reference statements)

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“…Bcl-2, an anti-apoptotic protein, significantly inhibited apoptosis and reduced the generation of ROS [ 177 ]; SIRT1 is a potential node for regulating DOX-induced cardiotoxicity and can prevent DOX-induced cardiac dysfunction through the oxidative stress pathway [ 178 ]. Xu et al [ 179 ] used miR-22 antagonists to significantly reduce the level of miR-22 and upregulate SIRT1 expression, which culminated in the reduction of DOX-induced oxidative stress damage to cardiomyocytes.…”

Section: Mirna As a Therapeutic Target Of Dicmentioning

confidence: 99%

MicroRNA in the Diagnosis and Treatment of Doxorubicin-Induced Cardiotoxicity

Kuang

Tan

et al. 2023

Biomolecules

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Doxorubicin (DOX), a broad-spectrum chemotherapy drug, is widely applied to the treatment of cancer; however, DOX-induced cardiotoxicity (DIC) limits its clinical therapeutic utility. However, it is difficult to monitor and detect DIC at an early stage using conventional detection methods. Thus, sensitive, accurate, and specific methods of diagnosis and treatment are important in clinical practice. MicroRNAs (miRNAs) belong to non-coding RNAs (ncRNAs) and are stable and easy to detect. Moreover, miRNAs are expected to become biomarkers and therapeutic targets for DIC; thus, there are currently many studies focusing on the role of miRNAs in DIC. In this review, we list the prominent studies on the diagnosis and treatment of miRNAs in DIC, explore the feasibility and difficulties of using miRNAs as diagnostic biomarkers and therapeutic targets, and provide recommendations for future research.

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Section: Mirna As a Therapeutic Target Of Dicmentioning

confidence: 99%

MicroRNA in the Diagnosis and Treatment of Doxorubicin-Induced Cardiotoxicity

Kuang

Tan

et al. 2023

Biomolecules

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“…et al reported another promising therapeutic target for DIC, namely tumor-suppressive human circular RNA CircITCH [ 37 ]. Other recent potential strategies that possibly reverse DIC include atg7 -based autophagy activation [ 38 ], meteorin-like (METRNL) protein [ 39 ], sirtuin 1 (SIRT1) [ 40 ], berberine [ 41 ], ADAR2 [ 42 ], elabela (ELA) [ 43 ], phenylalanine-butyramide (FBA) [ 44 ], gasdermin D [ 45 ], melatonin [ 46 ], levosimendan [ 47 ], paeonol [ 48 ], SNX17 [ 49 ], irisin [ 50 ], isorhapontigenin [ 51 ], liensinine [ 52 ], etc.…”

Section: Severe Neuropathy and Myopathy Side Effects In Chemotherapymentioning

confidence: 99%

The Battlefield of Chemotherapy in Pediatric Cancers

Wang

et al. 2023

Cancers

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The survival rate for pediatric cancers has remarkably improved in recent years. Conventional chemotherapy plays a crucial role in treating pediatric cancers, especially in low- and middle-income countries where access to advanced treatments may be limited. The Food and Drug Administration (FDA) approved chemotherapy drugs that can be used in children have expanded, but patients still face numerous side effects from the treatment. In addition, multidrug resistance (MDR) continues to pose a major challenge in improving the survival rates for a significant number of patients. This review focuses on the severe side effects of pediatric chemotherapy, including doxorubicin-induced cardiotoxicity (DIC) and vincristine-induced peripheral neuropathy (VIPN). We also delve into the mechanisms of MDR in chemotherapy to the improve survival and reduce the toxicity of treatment. Additionally, the review focuses on various drug transporters found in common types of pediatric tumors, which could offer different therapeutic options.

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“…SIRT1 overexpression or pharmacological activation attenuates DIC through various downstream targets. Specifically, pro-apoptotic p53, as well as p38 MAPK and p66shc, are inhibited by SIRT1, while the cardioprotective AMPK is activated by SIRT1 via liver kinase B1 (LKB1) and sestrin 2 action ( Zhang et al, 2011 ; Ruan et al, 2015 ; Wang et al, 2017 , 2022 ; Wu et al, 2019 ). In addition to the AMPK pathway, SIRT1 activates cardioprotective PGC-1α and nuclear factor erythroid 2-related factor 2 (NRF2).…”

Section: Mirnas Involved In the Inhibition Of Pro-survival Signaling ...mentioning

confidence: 99%

MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response

Kawano

Adamcová

2022

Front. Pharmacol.

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Doxorubicin (DOX) is a chemotherapeutic drug widely used for cancer treatment, but its use is limited by cardiotoxicity. Although free radicals from redox cycling and free cellular iron have been predominant as the suggested primary pathogenic mechanism, novel evidence has pointed to topoisomerase II inhibition and resultant genotoxic stress as the more fundamental mechanism. Recently, a growing list of microRNAs (miRNAs) has been implicated in DOX-induced cardiotoxicity (DIC). This review summarizes miRNAs reported in the recent literature in the context of DIC. A particular focus is given to miRNAs that regulate cellular responses downstream to DOX-induced DNA damage, especially p53 activation, pro-survival signaling pathway inhibition (e.g., AMPK, AKT, GATA-4, and sirtuin pathways), mitochondrial dysfunction, and ferroptosis. Since these pathways are potential targets for cardioprotection against DOX, an understanding of how miRNAs participate is necessary for developing future therapies.

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Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

Cited by 40 publications

References 54 publications

MicroRNA in the Diagnosis and Treatment of Doxorubicin-Induced Cardiotoxicity

MicroRNA in the Diagnosis and Treatment of Doxorubicin-Induced Cardiotoxicity

The Battlefield of Chemotherapy in Pediatric Cancers

MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response

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